Exercise-induced regulation of adipose tissue.

Exercise induces various beneficial whole-body adaptations and can delay the onset of obesity, type 2 diabetes, and cardiovascular disease. While many of the beneficial effects of exercise on skeletal muscle and the cardiovascular system have been well established, recent studies have highlighted the role of exercise-induced improvements to adipose tissue that affect metabolic and whole-body health. Studies investigating exercise-induced adaptations of white adipose tissue (WAT) and brown adipose tissue (BAT) demonstrate modifications to glucose uptake, mitochondrial activity, and endocrine profile, and a beiging of WAT in rodents. This review discusses recent studies of the exercise-induced adaptations to WAT and BAT and their implications.

Multitissue responses to exercise: a MoTrPAC feasibility study.

We assessed the feasibility of the Molecular Transducers of Physical Activity Consortium (MoTrPAC) human adult clinical exercise protocols, while also documenting select cardiovascular, metabolic, and molecular responses to these protocols. After phenotyping and familiarization sessions, 20 subjects (25 ± 2 yr, 12 M, 8 W) completed an endurance exercise bout (n = 8, 40 min cycling at 70% V̇o2max), a resistance exercise bout (n = 6, ∼45 min, 3 sets of ∼10 repetition maximum, 8 exercises), or a resting control period (n = 6, 40 min rest). Blood samples were taken before, during, and after (10 min, 2 h, and 3.5 h) exercise or rest for levels of catecholamines, cortisol, glucagon, insulin, glucose, free fatty acids, and lactate. Heart rate was recorded throughout exercise (or rest). Skeletal muscle (vastus lateralis) and adipose (periumbilical) biopsies were taken before and ∼4 h following exercise or rest for mRNA levels of genes related to energy metabolism, growth, angiogenesis, and circadian processes. Coordination of the timing of procedural components (e.g., local anesthetic delivery, biopsy incisions, tumescent delivery, intravenous line flushes, sample collection and processing, exercise transitions, and team dynamics) was reasonable to orchestrate while considering subject burden and scientific objectives. The cardiovascular and metabolic alterations reflected a dynamic and unique response to endurance and resistance exercise, whereas skeletal muscle was transcriptionally more responsive than adipose 4 h postexercise. In summary, the current report provides the first evidence of protocol execution and feasibility of key components of the MoTrPAC human adult clinical exercise protocols. Scientists should consider designing exercise studies in various populations to interface with the MoTrPAC protocols and DataHub.NEW & NOTEWORTHY This study highlights the feasibility of key aspects of the MoTrPAC adult human clinical protocols. This initial preview of what can be expected from acute exercise trial data from MoTrPAC provides an impetus for scientists to design exercise studies to interlace with the rich phenotypic and -omics data that will populate the MoTrPAC DataHub at the completion of the parent protocol.

Human adipose and skeletal muscle tissue DNA, RNA, and protein content.

The purpose of this project was to provide a profile of DNA, RNA, and protein content in adipose tissue, which is relatively understudied in humans, to gain more insight into the amount of tissue that may be required for various analyses. Skeletal muscle tissue was also investigated to provide a direct comparison into potential differences between these two highly metabolically active tissues. Basal adipose and skeletal muscle tissue samples were obtained from 10 (7 M, 3 W) recreationally active participants [25 ± 1 yr; 84 ± 3 kg, maximal oxygen consumption (V̇o2max): 3.5 ± 0.2 L/min, body fat: 29 ± 2%]. DNA, RNA, and protein were extracted and subsequently analyzed for quantity and quality. DNA content of adipose and skeletal muscle tissue was 52 ± 14 and 189 ± 44 ng DNA·mg tissue-1, respectively (P < 0.05). RNA content of adipose and skeletal muscle tissue was 46 ± 14 and 537 ± 72 ng RNA·mg tissue-1, respectively (P < 0.05). Protein content of adipose and skeletal muscle tissue was 4 ± 1 and 177 ± 10 µg protein·mg tissue-1, respectively (P < 0.05). In summary, human adipose had 28% of the DNA, 9% of the RNA, and 2% of the protein found in skeletal muscle per mg of tissue. This information should be useful across a wide range of human clinical investigation designs and various laboratory analyses.NEW & NOTEWORTHY This investigation studied DNA, RNA, and protein contents of adipose and skeletal muscle tissues from young active individuals. A series of optimization steps were investigated to aid in determining the optimal approach to extract high-yield and high-quality biomolecules. These findings contribute to the knowledge gap in adipose tissue requirements for molecular biology assays, which is of increasing importance due to the growing interest in adipose tissue research involving human exercise physiology research.

Influence of low-dose aspirin, resistance exercise, and sex on human skeletal muscle PGE2 /COX pathway activity.

Prostaglandin (PG) E2  has been linked to increased inflammation and attenuated resistance exercise adaptations in skeletal muscle. Nonaspirin cyclooxygenase (COX) inhibitors have been shown to reduce these effects. This study examined the effect of low-dose aspirin on skeletal muscle COX production of PGE2 at rest and following resistance exercise. Skeletal muscle (vastus lateralis) biopsies were taken from six individuals (4 M/2 W) before and 3.5 hr after a single bout of resistance exercise for ex vivo PGE2 production under control and low (10 µM)- or standard (100 µM)-dose aspirin conditions. Sex-specific effects of aspirin were also examined by combining the current findings with our previous similar ex vivo skeletal muscle investigations (n = 20, 10 M/10 W). Low-dose aspirin inhibited skeletal muscle PGE2 production (p < 0.05). This inhibition was similar to standard-dose aspirin (p > 0.05) and was not influenced by resistance exercise (p > 0.05) (overall effect: -18 ± 5%). Men and women had similar uninhibited skeletal muscle PGE2 production at rest (men: 1.97 ± 0.33, women: 1.96 ± 0.29 pg/mg wet weight/min; p > 0.05). However, skeletal muscle of men was 60% more sensitive to aspirin inhibition than women (p < 0.05). In summary, the current findings 1) confirm low-dose aspirin inhibits the PGE2 /COX pathway in human skeletal muscle, 2) show that resistance exercise does not alter aspirin inhibitory efficacy, and 3) suggest the skeletal muscle of men and women could respond differently to long-term consumption of low-dose aspirin, one of the most common chronically consumed drugs in the world.

Low-dose aspirin and COX inhibition in human skeletal muscle.

Skeletal muscle health has been shown to benefit from regular consumption of cyclooxygenase (COX)-inhibiting drugs. Aspirin, especially at low doses, is one of the most commonly consumed COX inhibitors, yet investigations of low-dose aspirin effects on skeletal muscle are nonexistent. The goal of this study was to examine the efficacy of low-dose aspirin on skeletal muscle COX production of the inflammatory regulator prostaglandin (PG)E2 at rest and after exercise. Skeletal muscle biopsies (vastus lateralis) were taken from eight individuals [4 men, 4 women; 25 ± 1 yr; 81.4 ± 3.4 kg; maximal oxygen consumption (V̇o2max): 3.33 ± 0.21 L/min] before and 3.5 h after 40 min of cycling at 70% of V̇o2max for the measurement of ex vivo PGE2 production. Muscle strips were incubated in Krebs-Henseleit buffer (control) or supplemented with one of two aspirin concentrations that reflected blood levels after a low (10 µM; typical oral dose: 75-325 mg) or standard (100 µM; typical oral dose: 975-1,000 mg) dose. Low (-22 ± 5%)- and standard (-28 ± 5%)-dose aspirin concentrations both reduced skeletal muscle PGE2 production, independent of exercise (P < 0.05). There was no difference in PGE2 suppression between the two doses (P > 0.05). In summary, low-dose aspirin levels are sufficient to inhibit the COX enzyme in skeletal muscle and significantly reduce production of PGE2, a known regulator of skeletal muscle health. Aerobic exercise does not appear to alter the inhibitory efficacy of aspirin. These findings may have implications for the tens of millions of individuals who chronically consume low-dose aspirin.NEW & NOTEWORTHY This study demonstrated that even low-dose aspirin concentrations can significantly reduce the prostaglandin (PG)E2/cyclooxygenase (COX) pathway activity in human skeletal muscle and this effect is not altered during the recovery period following aerobic exercise. These findings are noteworthy since aspirin is one of the most commonly consumed drugs in the world and nonaspirin COX-inhibiting drugs have been shown to regulate skeletal muscle health in sedentary and exercise-training individuals.